Anais Brasileiros de Dermatologia 2022;97(2):166---172

Anais Brasileiros de
Dermatologia
www.anaisdedermatologia.org.br

ORIGINAL ARTICLE

Pediatric androgenetic alopecia: a retrospective

review of clinical characteristics, hormonal assays and
metabolic syndrome risk factors in 23 patients夽
Deren Özcan

Department of Dermatology, Başkent University Faculty of Medicine, Ankara, Turkey

Received 13 May 2021; accepted 28 June 2021

Available online 13 January 2022

Abstract
KEYWORDS
Background: Androgenetic alopecia in the pediatric population is rarely discussed in the lit-
Adolescents;
erature. Although the prevalence of the metabolic syndrome is increased in patients with
Androgenetic
early-onset androgenetic alopecia, the presence of metabolic syndrome risk factors in pediatric
alopecia;
androgenetic alopecia is unknown.
Children;
Objective: To evaluate the demographics, medical and family histories, clinical and tri-
Metabolic syndrome
choscopic features, androgenic hormones, and metabolic syndrome risk factors in pediatric
androgenetic alopecia.
Methods: The medical reports of pediatric patients with androgenetic alopecia were reviewed.
Results: The study included 23 patients (12 females and 11 males) with a mean age of 15,3 ± 2,1
years. Sixteen patients had adolescent androgenetic alopecia and seven, had childhood alope-
cia. Nine patients reported a family history, all of whom had adolescent androgenetic alopecia.
Hyperandrogenism was noted in three patients with adolescent androgenetic alopecia. The most
common hair loss pattern was diffuse thinning at the crown with preservation of the frontal
hairline which was noted in 10 patients (43.5%), six of whom were males. Fourteen patients
(60.9%) had at least one metabolic syndrome risk factor. The most common risk factor was
obesity or overweight (47.8%) followed by insulin resistance (21.7%), high fasting blood glucose
(13%), high blood pressure (4.4%) and lipid abnormalities (4.4%).

夽 Study conducted at the Department of Dermatology, Başkent University Faculty of Medicine, Ankara, Turkey.
E-mail: derenozcan@yahoo.com.tr

https://doi.org/10.1016/j.abd.2021.06.006
0365-0596/© 2021 Sociedade Brasileira de Dermatologia. Published by Elsevier España, S.L.U. This is an open access article under the CC
BY license (http://creativecommons.org/licenses/by/4.0/).
 Anais Brasileiros de Dermatologia 2022;97(2):166---172

Study limitations: Retrospective study; lack of a control group.

Conclusion: Pediatric androgenetic alopecia is often associated with metabolic syndrome risk
factors. Therefore, androgenetic alopecia in the pediatric population may indicate a future
metabolic syndrome which warrants an accurate and prompt diagnosis for early screening and
treatment.
© 2021 Sociedade Brasileira de Dermatologia. Published by Elsevier España, S.L.U. This is an
open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

Introductıon The medical records of 23 pediatric patients diagnosed

In children and adolescents, alopecia areata and tri-
chotillomania are reportedly the most common forms of
alopecia, but Androgenetic Alopecia (AGA) is suggested
to be more frequent than was previously anticipated.1---3
Both androgenic hormones and genetic predisposition have
a role in AGA development, and the onset is therefore
not expected in prepubertal patients without abnormal
androgen levels.3---5 Over the last century, the onset of
adrenarche and puberty have shifted toward younger ages,
most probably due to hyperinsulinemic diet and increased
environmental hormonal, and sexual exposure.4,5 Thus, it is
proposed that the prevalence of pediatric AGA is increased
as this population is exposed to increased levels of cir-
culating androgens at younger ages which leads to early
development of AGA in genetically susceptible children.2,4
Owing to its predilection for adults, AGA in the pedi-
atric population is usually under-recognized, thus rarely
discussed in the literature. Therefore, little is known about
the natural history, clinical and trichoscopic characteris-
tics, and associated diseases and hormonal abnormalities in
pediatric patients with AGA.1---7 Free and total testosterone,
dehydroepiandrosterone sulphate (DHEAS), and androstene-
dione are the most commonly evaluated androgens in
those patients.1---3,5 AGA, in itself, has been reported to be
associated with many metabolic-related diseases such as
metabolic syndrome (MetS), cardiovascular disease (CVD),
insulin resistance (IR), hypertension, dyslipidemia, and obe-
sity in adults.8---15 Among them, MetS has received greater
interest, and its prevalence has been found to be increased
especially in patients with early-onset (age <35 years)
AGA.9---13,15 However, the presence of MetS or its risk factors
in pediatric AGA has not been investigated before.
AGA is a life-long genetic process that may also affect the
pediatric population. Therefore, it is critical to know its clin-
ical presentation with the potential associated hormonal and
metabolic abnormalities in this group of patients for timely
diagnosis, appropriate medical intervention, and treatment.
In this retrospective study, we evaluated the demographics,
medical and family histories, clinical features along with the
trichoscopic findings, androgenic hormones, and risk factors
for MetS in pediatric patients with AGA.
Methods
This study was approved by the Başkent University Institu-
tional Review Board (Project no: KA 21/137), and all patients
gave informed consent for the publication of their data.
with AGA between December 2015 and June 2020 were
reviewed retrospectively. The diagnosis of AGA was made by
the characteristic patterned alopecia and the trichoscopic
presence of >20% hair diameter diversity. The hair-pull test,
trichoscopy, and laboratory examination (total blood cell
count, blood levels of ferritin, and thyroid-stimulating hor-
mone) were performed; the triggering factors (high fever,
major surgical intervention, drugs, heavy diet, emotional
stress) were questioned to exclude telogen effluvium and
diffuse alopecia areata.
The patients’ ages and gender, medical and family
history, age at disease onset, duration of AGA, and asso-
ciated dermatological diseases were noted. The clinical and
trichoscopic findings were recorded. The images were re-
evaluated, and previously unrecorded features, if any, were
added. The results of total blood cell count, blood levels of
ferritin, thyroid-stimulating hormone, free and total testos-
terone, DHEAS, androstenedione, triglycerides, high-density
lipoprotein (HDL) cholesterol, total cholesterol, low-density
lipoprotein (LDL) cholesterol and fasting blood glucose, and
homeostasis model assessment of insulin resistance (HOMA-
IR) were recorded.
On their first admission, all the pediatric patients
diagnosed with AGA were referred to pediatrics for
the evaluation of sexual development and an underly-
ing endocrine disorder. The blood pressure, body mass
index (BMI), presence of early puberty, and signs of hir-
sutism or virilization were all recorded. The diagnosis of an
endocrine or cardiovascular disorder such as diabetes melli-
tus, hyperandrogenism, polycystic ovary syndrome (PCOS),
hyperlipidemia, hypertension, or MetS, if made, were also
noted.
MetS risk factors were particularly noted for each patient
as previously described.16,17 These included IR (HOMA-IR
>2.7), high fasting blood glucose (>100 mg/dL), overweight
(BMI 25---30 kg/m2 ) or obesity (BMI ≥ 30kg/m2 ), high blood
pressure (≥130/85 mmHg), and lipid abnormalities (triglyc-
erides >150 mg/dL or HDL cholesterol <40 mg/dL).
Pediatric AGA was classified as childhood AGA and ado-
lescent AGA if the onset occurred before puberty and
postpubertal, respectively. For this purpose, we questioned
the patients or their parents for the existence of breast
development, pubic and axillary hair growth, menstrua-
tion, and ejaculation at the time of the beginning of hair
loss. If we were unable to determine the pubertal status
at the age of AGA onset, we defined an adolescent by age
older than ten years (as proposed by World Health Organi-
zation).

167
 D. Özcan
Results
The study included 12 females and 11 males with a mean age
of 15.3 ± 2.1 years (range, 10---21 years). Sixteen patients
had adolescent AGA (eight females and eight males; mean
age: 16.3 ± 2.3 years; range, 11---21 years), and seven
patients had childhood AGA (four females and three males;
mean age: 12.9 ± 2.1 years; range 12---19 years). Table 1 dis-
plays age at presentation, age at onset, and duration of
AGA.
A family history of patterned hair loss in a first-degree
relative was present in nine (56.3%) of 16 patients with ado-
lescent AGA (six males, three females). Six males had only
their father, and two females had only their mother, and one
female had both parents affected. One of the two males
with no family history of AGA had associated acne, while
the other had no clinical or laboratory abnormality. None of
the patients with childhood AGA reported a family history in
the first-degree relatives. Two females with adolescent AGA
had a previous history of IR, and one female with adolescent
AGA reported a previous history of PCOS. One of the females
with IR also had associated hypertension.
Concurrent dermatological diseases were observed in 11
(47.8%) of 23 patients. Of those, eight patients (72.7%)
(five males, three females) and three patients (27.3%) (two
females, one male) had acne and seborrheic dermatitis,
respectively. Hirsutism was noted in two females, one of
whom also had seborrheic dermatitis. One of the males with
acne and one of the females with seborrheic dermatitis, who
were adolescents at initial presentation, had childhood AGA.
The patients’ sexual development and growth parameters
were appropriate for their ages except for the female with
early puberty, hirsutism, and seborrheic dermatitis.
The most common hair loss pattern was diffuse thin-
ning at the crown with preservation of the frontal hairline
(Figs. 1A and 1B) and was noted in 10 (43.5%) of 23 patients
with pediatric AGA. It was followed by ‘‘Christmas tree’’
pattern (Fig. 2A) in four (17.4%), bitemporal, frontoparietal,
and vertex thinning (Fig. 2B) in three (13%), diffuse thinning
pronounced at the crown with bitemporal thinning in three
(13%), bitemporal and vertex thinning in two (8.7%) patients,
and diffuse thinning pronounced at the crown in one patient
(4.4%). The hair pull test was negative in all patients. Six
(54.5%) of 11 males had diffuse thinning at the crown with
preservation of the frontal hairline. Among the females, the
most frequent clinical presentations were diffuse thinning
at the crown with preservation of the frontal hairline and
‘‘Christmas tree’’ pattern, each observed in four (33.3%) of
12 females (Table 2).
Trichoscopy (Figs. 3A and 3B) showed >20% hair diame-
ter diversity in all 23 (100%) patients. Additional findings
were vellus hairs (91.3%), single-hair pilosebaceous units
(34.8%), perifollicular discoloration (30.4%), yellow dots
(30.4%), wavy hair (26.1%), circle hair (13%), dotted ves-
sels (13%), honeycomb pigmentation (4.4%), thin arborizing
vessels (4.4%), and comma vessels (4.4%) (Table 2).
Fourteen patients (60.9%) with pediatric AGA (10 adoles-
cent and four childhood AGA, eight females and six males)
had at least one of the risk factors of MetS. Obesity or over-
weight was the sole MetS risk factor in eight patients (34.8%)
(five adolescent and three childhood AGA, six females and
168
five males). Of the remaining five patients with adolescent
AGA, two were obese or overweight and had IR, one of whom
also had hypertension, and two had high fasting blood glu-
cose and IR, and one was obese and had high fasting blood
glucose. One patient with childhood AGA had IR and lipid
abnormalities (Table 3). Of the five patients with IR, three
were females, and two were males. All three patients with
high fasting blood glucose and one patient who had high
blood pressure were females. The only patient with lipid
abnormalities was a male.
Other laboratory investigations showed increased total
cholesterol levels in five patients (three childhood and two
adolescent AGA), two of whom with childhood AGA also
had increased LDL cholesterol levels. Of those five patients,
three were obese or overweight. Blood levels of free and
total testosterone and androstenedione were increased in
two patients (one female and one male) and one female,
respectively, all of whom had adolescent AGA. One patient
with an increased blood level of free and total testosterone
was overweight. The results of total blood cell count, blood
levels of ferritin, thyroid-stimulating hormone, and DHEAS
were within normal levels.
Dıscussıon
Although pediatric AGA has rarely been reported in the liter-
ature, it is presumably not exceptional.1,3,5---7 In the pediatric
population, AGA usually starts in adolescence but has also
been reported to occur in prepubertal age.1---3,5---7 Gonzalez
et al.1 reported that, of the 438 pediatric patients com-
plaining of hair loss, 57 patients were diagnosed with AGA,
which was identified as the second most common diagno-
sis following alopecia areata in this population. Of those
57 patients, 52 patients were in adolescence, and AGA was
the most prevalent type of alopecia in adolescents occur-
ring in 42%. Additionally, a male predominance was noted
overall and also in adolescent patients. Kim et al.5 observed
43 adolescents with AGA over a period of nearly five years,
and males outnumbered females in their study, too. In both
studies, age at onset and initial presentation were slightly
higher in males rather than females.1,5 In the series of Gon-
zalez et al.,1 males had a shorter delay to diagnosis, while
Kim et al.5 reported a longer disease duration in males.
Tosti et al.3 diagnosed 20 prepubertal children within four
years. In their series, contrasting with the adolescent data,
AGA was more frequent in females but started, and patients
sought care at similar ages in both sexes. In their study, the
youngest age at onset was six years, yet AGA was reported to
begin in a patient as young as 5 years old.3,7 Similar to previ-
ous data, in our series of pediatric patients, AGA was more
common among adolescents. However, males and females
were affected with similar frequency overall, also during
adolescence and prepubertal ages. Differing from previous
reports, age at initial presentation and AGA duration were
higher in females, both in adolescent and childhood AGA.
Age at onset was remarkably close to each other in males
and females in adolescent AGA, while hair loss began at an
older age in males with childhood AGA. Similar to previous
reports, the earliest onset of AGA was 5 years of age in our
study.
 Anais Brasileiros de Dermatologia 2022;97(2):166---172

Table 1 Age at presentation, age at onset, and duration of AGA in 16 patients with adolescent AGA, in seven patients with
childhood AGA, and in a total of 23 patients with pediatric AGA.

Patients Age at presentation, years (mean ± SD) Age at onset, years (mean ± SD) Duration, years (mean ± SD)
Pediatric AGA, n = 23 15.3 ± 2.1 12.1 ± 3.1 3.1 ± 2.2
Females, n = 12 15.8 ± 3.6 11.8 ± 3.6 4.0 ± 2.5
Males, n = 11 14.6 ± 2.1 12.5 ± 2.6 2.1 ± 1.2
Adolescent AGA, n = 16 16.3 ± 2.3 13.9 ± 1.6 2.4 ± 1.5
Females, n = 8 17 ± 3.1 13.9 ± 2 3.2 ± 1.7
Males, n = 8 15.6 ± 0.1 13.9 ± 1.1 1.6 ± 0.6
Childhood AGA, n = 7 12.9 ± 2.1 8.1 ± 1.5 4.7 ± 2.7
Females, n = 4 13.5 ± 1.9 7.8 ± 1.9 5.8 ± 3.1
Males, n = 3 12 ± 2 8.7 ± 0.6 3.3 ± 1.5

AGA, Androgenetic Alopecia; n, number.

Figure 1 Hair loss patterns observed in pediatric androgenetic alopecia. (A), Diffuse thinning at the crown with preservation
of the frontal hairline in a female with adolescent androgenetic alopecia. (B), Preservation of the frontal hairline in a male with
adolescent androgenetic alopecia who has diffuse thinning at the crown.

Figure 2 Hair loss patterns observed in pediatric androgenetic alopecia. (A), ‘‘Christmas tree’’ pattern in a female with adolescent
androgenetic alopecia. (B), Bitemporal, frontoparietal and vertex thinning in a male with adolescent androgenetic alopecia.

Figure 3 Trichoscopic findings of pediatric androgenetic alopecia. (A and B), Hair diameter diversity and single-hair pilosebaceous
units. (A), Perifollicular discoloration (white arrows). (B), Wavy hair (white arrows), circle hair (yellow arrows), dotted and comma
vessels (black arrows).

169
 D. Özcan

Table 2 Clinical and trichoscopic findings in 16 patients with adolescent AGA and in seven patients with childhood AGA.

Findings Adolescent AGA, n (%) Childhood AGA, n (%)

Clinical findings
Diffuse thinning at the crown with preservation of the frontal hairline 6 (43.8) (3 M, 3 F) 4 (57.1) (3 M, 1 F)
‘‘Christmas tree’’ pattern 3 (18.8) (3 F) 1 (14.3) (1 F)
Bitemporal, frontoparietal and vertex thinning 3 (18.8) (3 M) 0
Diffuse thinning pronounced at the crown with bitemporal thinning 1 (6.3) (1 F) 2 (28.6) (2 F)
Bitemporal and vertex thinning 2 (12.5) (2 M) 0
Diffuse thinning pronounced at the crown 1 (6.3) (1 F) 0
Trichoscopic findings
>20% hair diameter diversity 16 (100) 7 (100)
Vellus hairs 14 (87.5) 7 (100)
Single-hair pilosebaceous units 6 (37.5) 2 (28.6)
Perifollicular discoloration 7 (4.8) 0
Yellow dots 6 (37.5) 1 (14.3)
Wavy hair 5 (31.3) 1 (14.3)
Circle hair 3 (18.8) 0
Dotted vessels 3 (18.8) 0
Honeycomb pigmentation 1 (6.3) 0
Thin arborizing vessels 1 (6.3) 0
Comma vessels 1 (6.3) 0

AGA, Androgenetic Alopecia; F, Female; M, Male; n, number.

Table 3 MetS risk factors in 16 patients with adolescent AGA, in seven patients with childhood AGA and in a total of 23 patients
with pediatric AGA.

MetS risk factors Adolescent AGA, n (%) Chilhood AGA, n (%) Total, n (%)
2
Overweight (BMI 25---30kg/m ) or obesity 8 (50) 3 (42.9) 11 (47.8)
(BMI ≥ 30 kg/m2 )
IR (HOMA-IR >2.7) 4 (25) 1 (14.3) 5 (21.7)
High fasting blood glucose (>100 mg/dL) 3 (18.8) 0 3 (13)
High blood pressure (≥130/85 mmHg) 1 (6.3) 0 1 (4.4)
Lipid abnormalities (triglycerides >150 mg/dL or HDL 0 1 (14.3) 1 (4.4)
cholesterol <40 mg/dL)

AGA, Androgenetic Alopecia; BMI, Body Mass Index; HDL, High Density Lipoprotein; HOMA-IR, Homeostasis Model Assessment of Insulin
Resistance; n, number; IR, Insulin Resistance; MetS, Metabolic Syndrome.

In men and some women, AGA results from dihy-
drotestosterone action, the 5-alpha reduced metabolite of
testosterone, on a genetically susceptible hair follicle.4 Con-
sequently, follicular miniaturization in the frontotemporal
area and vertex in men and over the crown in women
occurs, as these areas are more sensitive to the effects of
androgens.4,13 Clinically, most adolescent males with AGA
exhibit hair thinning consistent with typical male pattern
hair loss, as seen in adult men.1,2,5 However, a female
pattern was recorded in 20% and 34% of males with ado-
lescent AGA in two different studies.1,5 Tosti et al. reported
in their series of prepubertal children that in both sexes,
AGA presented with a female pattern, consisting of thin-
ning and widening of the central parting of the scalp
with preservation of the frontal hairline.2 The observa-
tion of female pattern AGA in prepubertal children and
adolescent males raised the belief that AGA may not be
necessarily androgen-dependent, at least in some pediatric
patients.1,3,5 In concordance with the previous studies, we
also observed a female pattern in one-third of the males
with adolescent AGA and all males with childhood AGA. How-
ever, interestingly, two females with childhood AGA and one
female with adolescent AGA exhibited bitemporal thinning
in addition to diffuse thinning pronounced at the crown. Our
findings show that the clinical pattern of AGA in some of our
pediatric patients was contrary to adult patterns, with males
displaying a female pattern and females showing a male pat-
tern. However, this observation has no precise explanation
yet.
Trichoscopic findings in our pediatric patients with AGA
were similar to those observed in adults.18 Besides >20%
hair diameter diversity, which appears as a consequence
of follicular miniaturization, increased proportion of vellus
hairs, single-hair pilosebaceous units, perifollicular discol-
oration, yellow dots, and wavy hair were the most frequent
findings. Trichoscopy also showed circle hair, honeycomb
pigmentation, and most probably due to associated seb-
orrheic dermatitis or as a normal scalp finding, dotted,
comma, or thin arborizing vessels.
AGA is expected to begin after puberty when
enough testosterone is available to be transformed
into dihydrotestosterone.1---3,5---7 As prepubertal children

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 Anais Brasileiros de Dermatologia 2022;97(2):166---172
normally do not produce sufficient amounts of adrenal and
gonadal androgens, the observation of AGA may indicate
a hormonal abnormality in those patients.1---5 However, the
study of Tosti et al.,3 a case report7 and likewise our study
showed that AGA is not associated with increased blood
levels of androgenic hormones beyond that expected for
the stage of sexual development in prepubertal children.
This observation suggests that AGA in children may not be
gonadal androgen driven or that adrenal androgens may
have a direct role.1,3,7 The adrenal secretion of androgen
hormones begins to increase 2---3 years before puberty
onset, called adrenarche, which occurs independently from
gonadal maturation.3 It is proposed that the strong genetic
predisposition, a characteristic common to the patients
from the previous reports, could be responsible for an
increased androgen sensitivity, and thus adrenal androgens
may be adequate to induce AGA in predisposed children.1,3,4
The progressive lower age of onset of adrenarche could
favor this process.3,4 Yet, so far, the hypothesis of androgen
hypersensitivity of the hair follicle in AGA has not been
precisely proven in children and female pattern AGA.
Therefore, either in children or adult women, AGA may
have different pathogenetic pathways than the peculiarities
of androgen metabolism underlying male pattern hair loss.
In our study, none of our patients with childhood AGA had a
positive family history in their first-degree relatives which
also supports this suggestion.
AGA can sometimes be the sole dermatologic finding of
PCOS.2 Although elevated androgen levels are found in a
small subset of adolescent patients, PCOS is observed in
nearly half of the adolescent females with AGA.1,4 Strong
family history is also noted frequently in both adolescent
males and females with AGA.1,2,5 In the present study, in
accordance with the literature data, AGA was reported in
the first-degree relatives of more than half of our patients
and nearly all males with adolescent AGA. Moreover, associ-
ated acne, seborrheic dermatitis, or hirsutism, which reflect
the effects of androgens, were observed in nearly half of
our pediatric patients, almost all of whom had adolescent
AGA. However, hyperandrogenism was not a frequent find-
ing overall, and PCOS or early puberty was noted only in two
females. As proposed previously, we also think that, like
in children with prepubertal testosterone levels, adrenal
androgens might contribute to the development of AGA, or
it might have occurred by a mechanism completely indepen-
dent of the effect of androgenic hormones in our adolescent
females with normal hormone profiles.
MetS describes clustering of central obesity, disturbed
glucose metabolism, hypertension and dyslipidemia, and the
presence of three or more of these components significan-
tly increases the risk for developing CVD and diabetes.8,12,17
There are many studies that show the relationship between
AGA and MetS and its individual components in adults.8---15
In particular, early-onset of AGA in adults (before the
age of 35 years) has been shown to be a risk factor
for early onset of severe CVD, and some studies found
a higher prevalence of IR and MetS in this group of
patients.8,11,13,15 The underlying mechanism linking AGA and
MetS has not been fully established. However, it has been
claimed that IR, the key mechanism in the development
of MetS, could also contribute to AGA.8,13,19 Hyperinsuline-
mia may play a role in local androgen production from
171
cholesterol and through local conversion of testosterone
to dihydrotestosterone.8,19 Vasoactive substances produced
in IR further cause vasoconstriction and tissue hypoxia at
the follicular level and contribute to the miniaturization
of hair follicles.8,13,19 Moreover, high serum androgen levels
and peripheral sensitivity to androgens observed in AGA may
increase the risk of developing hypertension via androgen-
mediated receptors found in the arterial wall endothelium
and play an additional role in the association of AGA and
MetS.8,13
As in adulthood, obesity, and hence IR in childhood and
adolescence, poses a growing problem, and pediatricians
have increasingly diagnosed MetS in recent years.20,21 Suf-
fering from MetS and its risk factors during the pediatric
age does not predict that they will persist in adulthood.20
Yet, the importance of early identification of children and
adolescents at risk of developing MetS and subsequently
progressing to diabetes and CVD in later life must not be
underestimated.20,21 Despite many studies in adults exist,
the association of AGA and MetS in the pediatric population
is yet to be investigated. In our study, more than half of
the pediatric patients with AGA exhibited at least one MetS
risk factor. The frequency of these risk factors was similar
in females and males. Obesity or overweight, the most com-
mon cause of IR and the major determinant of MetS,16,17,19
was observed in nearly half of the patients and was the
sole risk factor for one-third. IR and high fasting glucose
which are the signs of disturbed glucose metabolism, were
the second most commonly noted MetS risk factors. Other
risk factors, including hypertension and lipid abnormalities,
were infrequent in our pediatric patients. As our study did
not have a control group, it is hard to determine whether a
true association between pediatric AGA and the presence of
MetS risk factors exists or not. However, we think that our
findings are critical to underline the necessity for screen-
ing pediatric patients with AGA for the risk factors of MetS
since most of these disorders are asymptomatic but related
to later CVD and diabetes.
The retrospective nature and the lack of a control group
were the main limitations of the current study. Additionally,
the findings observed in adolescent and childhood AGA and
also in females and males could not be statistically com-
pared due to the insufficient number of patients.
Conclusıon
The results of our study show that AGA is more prevalent
among adolescents than children in the pediatric population
and presents with clinical and trichoscopic features simi-
lar to those reported previously. Hyperandrogenism is not
a common finding and probably does not contribute to the
occurrence of AGA in the majority of children and adoles-
cents. In contrast, genetic predisposition may play a role in
adolescent AGA. Pediatric patients with AGA often present
with at least one of the risk factors of MetS. Hence, we think
that AGA in pediatric patients may be a sign of a future MetS,
and therefore warrants an accurate and prompt diagnosis
for early screening and halting the progression of this syn-
drome. Prospective controlled studies will better clarify the
association of pediatric AGA with MetS risk factors.
 D. Özcan
Financial support
None declared.
Authors’ contributions
Deren Özcan: Approval of the final version of the manuscript;
critical literature review, data collection, analysis, and
interpretation; effective participation in research orienta-
tion intellectual participation in propaedeutic and/or ther-
apeutic management of studied cases; critical manuscript
review; preparation and writing of the manuscript, study
conception, and planning.
Conflicts of interest
None declared.
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